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Clearance systems in the brain-implications for Alzheimer disease. 1.0.1

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Provenance

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charles.hoyt@scai.fraunhofer.de at 2019-02-27 16:23:20.501740
Authors
Lingling Xu
Contact
charles.hoyt@scai.fraunhofer.de
License
CC BY 4.0
Copyright
Copyright © 2018 Fraunhofer Institute SCAI, All rights reserved.
Number Nodes
83
Number Edges
123
Number Components
3
Network Density
0.0180722891566265
Average Degree
1.48192771084337
Number Citations
1
Number BEL Errors
0

Content Statistics

Network Overlap

The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.

Network Overlap
Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0 33%
Identification of a novel aspartic protease (Asp 2) as beta-secretase v1.0.0 30%
Effects of peptides derived from BACE1 catalytic domain on APP processing v1.0.0 30%
Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1 28%
Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0 25%
Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. v1.0.0 25%
Pseudophosphorylation of tau at S422 enhances SDS-stable dimer formation and impairs both anterograde and retrograde fast axonal transport. v1.0.0 20%
Anatabine lowers Alzheimer's Aβ production in vitro and in vivo v1.0.0 20%
Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0 19%
Tau Trimers Are the Minimal Propagation Unit Spontaneously Internalized to Seed Intracellular Aggregation v1.0.0 18%

Sample Edges

p(HGNC:MAPT) hasVariant p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

g(HGNC:APP) hasVariant g(HGNC:APP, var("?")) View Subject | View Object

g(HGNC:PSEN1) hasVariant g(HGNC:PSEN1, var("?")) View Subject | View Object

g(HGNC:PSEN2) hasVariant g(HGNC:PSEN2, var("?")) View Subject | View Object

a(CHEBI:"amyloid-beta polypeptide 40") association path(MESH:"Alzheimer Disease") View Subject | View Object

Given the size of AD-related proteins, mono- meric Aβ1-40, Aβ1-42 and tau, should be able to pass freely through astrocytic endfeet clefts at the glial barrier.72 PubMed:26195256

Sample Nodes

a(CHEBI:"amyloid-beta")

In-Edges: 423 | Out-Edges: 245 | Children: 5 | Explore Neighborhood | Download JSON

a(MESH:Microglia)

In-Edges: 19 | Out-Edges: 25 | Explore Neighborhood | Download JSON

p(MGI:Aqp4)

In-Edges: 0 | Out-Edges: 5 | Explore Neighborhood | Download JSON

path(MESH:"Alzheimer Disease")

In-Edges: 536 | Out-Edges: 704 | Classes: 5 | Explore Neighborhood | Download JSON

path(MESH:Inflammation)

In-Edges: 83 | Out-Edges: 41 | Explore Neighborhood | Download JSON

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.